Central toxic keratopathy may occur after laser refractive surgery

This syndrome does not respond to topical corticosteroid therapy and also differs in other ways from DLK, according to Robert K. Maloney, MD.

"DLK is inflammatory while this [syndrome] is noninflammatory. DLK is diffuse while this is focal. DLK is confined to the interface while this extends posterior to the interface. DLK responds to steroids whereas this entity does not, and DLK cannot occur after PRK whereas this can," said Dr. Maloney, director of the Maloney Vision Institute in Los Angeles and clinical professor of ophthalmology at the University of California, Los Angeles. "For these reasons, central toxic keratopathy may be a preferable term to stage IV DLK," which some clinicians call this entity.

DLK is a well-known side effect of LASIK, and several authors have described a syndrome characterized by central opacification, stromal loss, striae, and reduced quality of vision. Eric J. Linebarger, MD, David R. Hardten, MD, and Richard L. Lindstrom, MD, labeled it stage IV DLK. While these authors have described differences as well as similarities in what they have observed, Dr. Maloney said he believes all were referring to the same condition, which he prefers to call central toxic keratopathy.

To study this syndrome, he and Dr. Sonmez reviewed a digital archive of clinical photographs from Dr. Maloney's clinic. Charts were reviewed and data abstracted from them retrospectively. Eligible eyes were those that developed noninflammatory central stromal opacification 2 to 9 days after laser treatment. The main outcome measures were change in best spectacle-corrected visual acuity (BSCVA), maximum hyperopia, time to clearing of the opacification, and additional procedures.

Twenty-three eyes of 14 patients with noninflammatory central corneal opacification in the immediate postoperative period after LASIK or PRK were identified. In this series, the opacification developed from 3 to 9 days after surgery, usually on postoperative days 3 to 6.

Nineteen of the eyes had LASIK, including two that had undergone the procedure with the femtosecond laser (IntraLase, Advanced Medical Optics/IntraLase Corp.), and four eyes of two patients had PRK. In all eyes, central corneal opacification developed in the area of laser treatment that extended posteriorly from the interface into the stromal bed (in the case of eyes that underwent LASIK). Opacification lasted from 2 to 18 months before clearing. Haze cleared within 1 year in most eyes. Dr. Maloney acknowledged, however, that some severe cases of central toxic keratopathy might take longer to clear or might never clear completely.

Only one eye in this retrospective series lost BSCVA. This eye presented with severe opacity at 20/40 and had improved to 20/25 a year later.

Syndrome characteristics

Describing characteristics of central toxic keratopathy, Dr. Maloney stated that the opacification is always central and can be mild to severe; striae are almost uniformly present and in this series were found in 16 of 19 eyes that underwent LASIK and one of the eyes that underwent PRK.

A hyperopic shift consistent with the degree of observed corneal thinning was present in many cases. Nine of 23 eyes developed at least 2 D of hyperopia, and it reached 12 D in one patient.

Stromal tissue loss appears to be characteristic of central toxic keratopathy and may be related to keratocyte apoptosis, Dr. Maloney said. The apoptosis causes significant volume loss, which, in turn, leads to the collapse of the central cornea and subsequent hyperopic shift. Another theory speculates that enzymatic degradation of the central stromal matrix causes central corneal collapse.